Metzner W
Department of Zoology, University of Munich, Germany.
J Neurosci. 1993 May;13(5):1899-915. doi: 10.1523/JNEUROSCI.13-05-01899.1993.
The control of vocalization depends significantly on auditory feedback in any species of mammals. Echolocating horseshoe bats, however, provide an excellent model system to study audio-vocal (AV) interactions. These bats can precisely control the frequency of their echolocation calls by monitoring the characteristics of the returning echo; they compensate for flight-induced Doppler shifts in the echo frequency by lowering the frequency of the subsequent vocalization cells (Schnitzler, 1968; Schuller et al., 1974, 1975). It was the aim of this study to investigate the neuronal mechanisms underlying this Doppler-shift compensation (DSC) behavior. For that purpose, the neuronal activity of single units was studied during spontaneous vocalizations of the bats and compared with responses to auditory stimuli such as playback vocalizations and artificially generated acoustic stimuli. The natural echolocation situation was simulated by triggering an acoustic stimulus to the bat's own vocalization and by varying the time delay of this artificial "echo" relative to the vocalization onset. Single-unit activity was observed before, during, and/or after the bat's vocalization as well as in response to auditory stimuli. However, the activity patterns associated with vocalization differed from those triggered by auditory stimuli even when the auditory stimuli were acoustically identical to the bat's vocalization. These neurons were called AV neurons. Their distribution was restricted to an area in the paralemniscal tegmentum of the midbrain. When the natural echolocation situation was stimulated, the responses of AV neurons depended on the time delay between the onset of vocalization and the beginning of the simulated echo. This delay sensitivity disappeared completely when the act of vocalization was replaced by an auditory stimulus that mimicked acoustic self-stimulation during the emission of an echolocation call. The activity of paralemniscal neurons was correlated with all parameters of echolocation calls and echoes that are relevant in context with DSC. These results suggest a model for the regulation of vocalization frequencies by inhibitory auditory feedback.
发声的控制在任何哺乳动物物种中都显著依赖于听觉反馈。然而，使用回声定位的马蹄蝠提供了一个研究听觉-发声（AV）相互作用的绝佳模型系统。这些蝙蝠可以通过监测返回回声的特征精确控制其回声定位叫声的频率；它们通过降低后续发声细胞的频率来补偿飞行引起的回声频率中的多普勒频移（施尼茨勒，1968年；舒勒等人，1974年、1975年）。本研究的目的是探究这种多普勒频移补偿（DSC）行为背后的神经元机制。为此，在蝙蝠自发发声期间研究了单个神经元的活动，并将其与对诸如回放叫声和人工生成的声学刺激等听觉刺激的反应进行了比较。通过触发与蝙蝠自身发声相关的声学刺激，并改变这个人工“回声”相对于发声开始的时间延迟，模拟了自然回声定位情况。在蝙蝠发声之前、期间和/或之后以及对听觉刺激的反应中观察到了单个神经元的活动。然而，即使听觉刺激在声学上与蝙蝠的发声相同，与发声相关的活动模式也与由听觉刺激触发的活动模式不同。这些神经元被称为AV神经元。它们的分布局限于中脑旁臂被盖区的一个区域。当模拟自然回声定位情况时，AV神经元的反应取决于发声开始与模拟回声开始之间的时间延迟。当发声行为被一种模仿回声定位叫声发射期间声学自我刺激的听觉刺激所取代时，这种延迟敏感性完全消失。旁臂神经元的活动与回声定位叫声和回声的所有与DSC相关的参数相关。这些结果提出了一个通过抑制性听觉反馈调节发声频率的模型。
